Abstract
The activities of 11β-hydroxysteroid dehydrogenase (11β-HSD) and 5β-reductase were analyzed in 39 normotensive controls and 128 patients with essential hypertension. The activity of 11β-HSD was obtained by dividing the 24-hour urinary tetrahydrocortisone by the sum of tetrahydrocortisol (THF) and allotetrahydrocortisol (aTHF), whereas the activity of 5β-reductase was obtained by dividing the 24-hour urinary THF by aTHF. The activity of 5β-reductase was significantly lower in essential hypertensives compared with normotensive controls ( P < 0.05). However, the activity of 11β-HSD did not differ between normotensive controls and essential hypertensives. A positive correlation between the activities of 11β-HSD and 5β-reductase was observed in essential hypersentives ( r = 0.60, P < 0.01). Neither 11β-HSD nor 5β-reductase activity correlated with indices of renal mineralocorticoid receptor activation, which were assessed by determination of plasma potassium and urinary excretion of sodium as well as potassium. Taken together, these results suggest that disturbances of one of the inactivation pathways of cortisol may contribute to the pathogenesis of hypertension.
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